Abstract：
:The pathogenesis of neurogenic pulmonary edema has been debated for many years. Whether cardiogenic mechanisms and increased pulmonary vascular pressures are primary or even necessary for the production of pulmonary edema has been argued. We used postictal pulmonary edema to study this problem in a sheep model of neurogenic pulmonary edema with bicucullin-induced status epilepticus. Seizure-induced increases in pulmonary vascular pressures were averted with a reservoir system to maintain left atrial pressure (LAP) and pulmonary artery pressure (PAP) at preseizure levels. No increase in lung lymph flow occurred during seizures, in contrast to the doubling of lung lymph flow that occurred during seizures when ictal pulmonary vascular hypertension was not blocked. These data support a primary role of pulmonary vascular pressure increases in the production of neurogenic pulmonary edema.
journal_name
Epilepsiajournal_title
Epilepsiaauthors
Johnston SC,Darragh TM,Simon RPdoi
10.1111/j.1528-1157.1996.tb00587.xsubject
Has Abstractpub_date
1996-05-01 00:00:00pages
428-32issue
5eissn
0013-9580issn
1528-1167journal_volume
37pub_type
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